Prenatal High‐Sucrose Diet Induced Vascular Dysfunction in Thoracic Artery of Fetal Offspring

Abstract

Scope Maternal nutrition during pregnancy is related to intrauterine fetal development. The authors’ previous work reports that prenatal high sucrose (HS) diet impaired micro‐vascular functions in postnatal offspring. It is unclear whether/how prenatal HS causes vascular injury during fetal life. Methods and results Pregnant rats are fed with normal drinking water or 20% high‐sucrose solution during the whole gestational period. Pregnant HS increases maternal weight before delivery. Fetal thoracic aorta is separated for experiments. Angiotensin II (AII)‐stimulated vascular contraction of fetal thoracic arteries in HS group is greater, which mainly results from the enhanced AT1 receptor (AT1R) function and the downstream signaling. Nifedipine significantly increases vascular tension in HS group, indicating that the L‐type calcium channels (LTCCs) function is strengthened. 2‐Aminoethyl diphenylborinate (2‐APB), inositol 1,4,5‐trisphosphate receptors (IP3Rs) inhibitor, increases vascular tension induced by AII in HS group and ryanodine receptors‐sensitive vascular tone shows no difference in the two groups, which suggested that the activity of IP3Rs‐operated calcium channels is increased. Conclusion These findings suggest that prenatal HS induces vascular dysfunction of thoracic arteries in fetal offspring by enhancing AT1R, LTCCs function and IP3Rs‐associated calcium channels, providing new information regarding the impact of prenatal HS on the functional development of fetal vascular systems.

Slower Growth during Lactation Rescues Early Cardiovascular and Adipose Tissue Hypertrophy Induced by Fetal Undernutrition in Rats

“…Perivascular WAT also plays a role in vascular tone and maintenance of normal structure [ 43 ], which is dysregulated by excess fat, as we have reported in obese mice [ 48 ]. A reduced proportion of beige-adipocytes may play a role in vascular dysfunction, an alteration observed in several animal models of fetal programming [ 49 ]. These alterations may be due to the pro-oxidant and proinflammatory environment associated with excess fat, favoring the local release of vasoactive factors.…”

Prenatal High‐Sucrose Diet Induced Vascular Dysfunction of Renal Interlobar Arteries in the Offspring via PPARγ‐RXRg‐ROS/Akt Signaling

“…The RIA was isolated and immediately fixed in 4% paraformaldehyde at 4 °C as described. [ 10 ] In brief, RIA was cut into 5‐mm sections and rehydrated with xylene and a descending alcohol. After washing with distilled water, the sections were stained with hematoxylin solution and eosin‐phloxlike B solution.…”

“…Pregnant rats in CON were provided with standard food and tap water, and the HS group was fed with the same food and 20% sucrose solution from gestational day 1-21. [10,[13][14][15][16] Caesarean delivery was conducted on pregnant rats at gestational day 21, and the fetal kidneys were obtained immediately. Other pregnant rats were vaginal delivery naturally.…”

“…[4][5][6][7] Notably, prenatal nutrition imbalance correlates with a greater risk of developmental origin of cardiovascular diseases. [8][9][10] An ever-growing evidence base demonstrates that high sugar/sucrose diet intake may increase deaths cases and cardiovascular disease burdens. [11,12] Therefore, much more attention should be paid to investigate the effects of high-sugar on vascular development, especially the gravida and fetus.…”

“…[13,14] Our previous study revealed that maternal high-sucrose diet altered vascular contraction in the offspring. [10,15,16] However, there has limited information on underlying mechanisms to interpret the association of prenatal high-sucrose diet with vascular diseases in renal interlobar arteries from the offspring.…”